Recent experimental data suggest a role for lipids in the pathogenesis
of glomerulosclerosis. In this study, we examined the main apolipopro
teins (apo) of high density lipoproteins (A-I, A-IV, E), low density l
ipoproteins (B), and very low density lipoproteins (B, E) in plasma an
d kidney tissue of rats with puromycin aminonucleoside or adriamycin n
ephrosis. In full-blown nephrosis, plasma concentrations of apo A-I an
d apo B were significantly elevated, apo A-I and apo E levels did not
change. Immunohistological studies in plastic sections retreated incre
ased apo A-I, apo A-IV, and apo E immunoreactivity in glomerular visce
ral epithelial cells both in puromycin aminonucleoside and adriamycin
nephrosis. This was confirmed by immunoelectronmicroscopy. In addition
, apo B and apo E were encountered in increased amounts in the mesangi
um and co-localized with Oil Red O-positive lipid deposits, particular
ly in puromycin aminonucleoside nephrosis rats. Double-staining showed
a preferential localization of apo B and apo E at sites of increased
mesangial matrix in close proximity to ED1-positive foam cells, i.e.,
the mesangial macrophages. The close topographic association between a
po B and apo E, lipid deposits, and macrophages in the mesangium lend
further support to the concept of lipid-mediated glomerular injury in
nephrosis.